The inflammatory response to acute cerebrovascular injury is a major determinant in stroke pathobiology and outcome. Inflammatory reactions occur early after the occurrence of both cerebral ischemia and haemorrhage. These reactions are mediated by a spectrum of inflammatory cells, cytokines, and inflammatory molecules, and may exacerbate the injury and contribute to secondary brain damage. Although detrimental during the acute phase of stroke, some inflammatory leukocytes have beneficial effects and contribute to tissue repair in the subacute stage by removing cell debris and secreting trophic factors. A bidirectional interaction also exists between the brain and peripheral immune systems. Indeed, although the immune response starts locally in the brain parenchyma, inflammatory mediators and brain-generated signals propagate through the organism and promote a systemic inflammatory response, followed by compensatory immunosuppression.

So far, one main challenge is the identification of mediators that result from the inflammatory mechanisms involved in brain injury. It can yield unreliable information on the progress of the disease. The identification of the biomarkers of the mechanisms underlying cerebral injury, including blood-brain barrier dysfunction, edema development, and brain cell death, as well post-stroke plasticity and regeneration would allow to improve the prediction of outcome and discover new targets of intervention.

This Special Issue aims to collate original research and review articles about the cellular and molecular basis of post-stroke inflammation. Submissions discussing the interactions between immune responses and secondary brain damage are also welcome. We also highly encourage research articles about the outcomes of a stroke with a focus on the identification and monitoring of mediators involved in inflammatory pathways. We hope that this Special Issue highlights existing knowledge gaps and expands our understanding of post-stroke inflammation at an experimental, translational or clinical level.

Potential topics include but are not limited to the following:

• Cellular and humoral mediators of inflammation after brain infarct and cerebral haemorrhage
• Peripheral biomarkers of inflammation and secondary brain injury after a stroke
• Relationship between mediators of inflammation and outcome after a stroke
• Crosstalk between mediators in the brain and mediators in the peripheral immune system
• Mediators that modulate a brain tissue repair after a stroke
• Effects of reperfusion therapies on mediators of inflammation in cerebral infarct
• Identification and characterization of potential therapeutic targets to modulate post-stroke inflammation